EMBARGOED FOR RELEASE UNTIL
APRIL 30, 2007
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Christine Guilfoy
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cguilfoy@the-aps.org
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Saturday April 28
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Your Brain And Hormones May
Conspire To Make You Fat
Washington — Why do some people get fat even
when they eat relatively little? What creates that irresistible urge for a
bag of potato chips or a hunk of chocolate cake, as opposed to a nice crisp
apple? Can food urges be irresistible?
Physiologists are unraveling the role that your
hormones and brain play in urging you to eat more than you should. Some
people’s hormones may be signaling their brains to send messages like “Eat a
lot now,” and “Go for the fat and sugar.”
Four physiologists will clarify the latest research on
the brain’s role in obesity, during the symposium, “Obesity and the
Central Nervous System.” The symposium will take place at the 120th
annual meeting of
The American Physiological Society
(APS), which coincides with Experimental Biology 2007. The
session will be held at 10:30 a.m., Monday, April 30 in Room 146B of the
Washington Convention Center and is cosponsored by the London-based
Journal of Physiology.
The body has a physiological predisposition to balance
its energy needs with its desire for food. The hormones and brain
communicate to determine when an individual is full, with the brain issuing
the signal that says “Stop eating” with the help of information it receives
from hormones. But prolonged food shortages, chronic stress, prenatal
nutrition, early exercise patterns and other factors can affect how the
brain orchestrates this balance. In places where food is scarce, the brain
may encourage higher consumption, especially of high fat and sugary foods,
even when the food supply becomes more abundant. That’s an adaptive response
that helps the body weather periods of food shortages.
But the brain may also respond to stress in the same
way, encouraging the intake of high fat and sugary foods – comfort foods -
that can result in obesity that is nearly impossible to reverse.
“Why some of us get fat and what we can do it about
it,” is the question Barry E. Levin, M.D., a professor at the New
Jersey Medical School of the University of Medicine and Dentistry of New
Jersey and of the Veterans Affairs Medical Center, East Orange, N.J., will
address.
The hormones leptin and insulin inhibit the development
of obesity when consumption of fat and calories increases. Some people
respond very well to these hormones and they don’t gain weight during these
bouts of overeating. But others are less responsive to leptin and insulin,
which makes them more at risk to become obese. Why? It appears that the
brain can be programmed to accept a higher body weight by early-life
factors, including the environment of the womb in late pregnancy and the
individual’s activity level in early life. These early factors may alter
development of brain pathways which regulate energy homeostasis (balance).
Once the tendency to obesity develops, it can be nearly impossible to
reverse weight gains. However, these early factors can be manipulated to
provide a more desirable outcome and may hold promise for prevention of
obesity in human beings.
“Glucocorticoids and insulin both modulate caloric
intake through actions on the brain,” is the topic for Mary F.
Dallman, Ph.D., a professor at the University of California in San
Francisco. Fat that develops in the abdomen to form a pot belly and thick
waist has been associated with more negative health outcomes (heart disease,
for example) than fat that accumulates in other areas of the body, such as
the hips. Glucocorticoids, a group of steroid hormones that includes
cortisol, activate a physiological process in the brain that matches the
desire for food with physiological need. Under conditions of inadequate food
or chronic stress, glucocorticoids prompt a craving for “comfort” foods –
foods high in sugar or fat. Glucocorticoids and insulin act to create
abdominal fat. That’s a good way to store energy during food shortages but
it’s also a way to gain too much abdominal fat when food is readily
available.
Gregory Morton, Ph.D., assistant professor of
medicine at Harborview Medical Center at the University of Washington,
Seattle will give a talk entitled “Hypothalamic leptin regulation of
energy homeostasis and glucose metabolism.” Insulin and leptin are
hormones that circulate in proportion to body fat stores. They interact with
receptors in key areas of the brain, including in the hypothalamic arcuate
nucleus, to regulate food intake and glucose metabolism. Morton and his
colleagues have recently shown that leptin signaling selectively in this
brain area is sufficient to reduce food intake and body weight and to
improve insulin sensitivity. These findings indicate that leptin signaling
in the arcuate nucleus is an important determinant of both energy
homeostasis and glucose metabolism.
Steven B.Heymsfield, M.D., is the executive
director of clinical research and metabolism at Merck & Co., Inc., in
Rahway, New Jersey. In his talk, “Development of an NPY5 receptor
antagonist for weight loss” he will review the development of MK-0557, a
drug designed to decrease food intake. MK-0557 blocks the effects of
neuropeptide Y 5 (NPY5), which is involved in food intake regulation. Merck
launched an intensive program leading to discovery of MK-0557 and then took
it through a series of investigations that supported safety and
effectiveness. A short-term weight loss study led to a large long-term
series of clinical trials. Many lessons in neurobiology and drug development
were learned from this progression of studies, the topic of the lecture.
***
The media
is invited to interview these speakers or to attend this conference, which
is expected to attract 14,000 scientists, by e-mailing
Christine Guilfoy or calling (301) 634-7253, prior to the
event. During the conference, please call the APS press room at (202)
249-4174. For reporters who cannot attend, arrangements can be made in many
cases for telephone interviews with scientists.
Please
click here for a summary of the APS program at Experimental Biology
2007.
Physiology
is the study of how molecules, cells, tissues and organs function to create
health or disease. The American Physiological Society has been an
integral part of this scientific discovery process since it was established
in 1887.
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